The anti-hyperglycemic effects of Cyclocarya paliurus polysaccharide (CPP) have attracted increasing attention; however, limited research has been conducted on the potential effects of CPP on inhibiting tumor growth. The present study aimed to investigate the functions of CPP in combination with X-ray irradiation on colorectal cancer cells and the underlying mechanisms. SW480 cells were treated with various concentrations of CPP for 24, 48 and 72 h to determine cell viability using a Cell Counting Kit-8 assay. Then, the cells were divided into four groups as follows: Control, CPP (100 µmol/l), 8 Gy and CPP + 8 Gy. The proliferation and apoptosis, and colony formation of cells were detected using flow cytometry and plate clone formation assays, respectively. Reverse transcription-quantitative PCR and western blot analyses were conducted to determine the expression of proliferation and apoptosis-associated, and PI3K/Akt signaling-associated genes. Treatment with 75 µmol/l CPP for 48 h significantly decreased cell viability compared with untreated cells. CPP in combination with 8 Gy X-ray treatment significantly promoted the induction of apoptosis, and suppressed cell proliferation and clone formation compared with the control, CPP and 8 Gy groups. The detection of mRNA and protein expression levels by reverse transcription-PCR and western blotting demonstrated that CPP in combination with 8 Gy not only significantly decreased the expression of proliferation marker protein Ki-67, p53 and Bcl-2, but also upregulated the expression of cleaved caspase-3 and Bax, compared with the control. In addition, CPP and 8 Gy combined significantly attenuated the phosphorylation of PI3K and Akt. The present study demonstrated that the combination of CPP with X-ray irradiation suppressed SW480 cell proliferation and promoted cell apoptosis compared with the control, CPP and 8 Gy groups. The underlying mechanisms may involve inhibition of PI3K/Akt signaling.

Objective. The purpose of this study was to study the effects of the GAS5/microRNA-10b (miR-10b) axis on proliferation, migration, and apoptosis of colorectal cancer (CRC). Methods. The expression levels of GAS5 and miR-10b in CRC tissues and cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Wound healing experiment was used to detect the effects of GAS5 and miR-10b on the migration of CRC cells. The luciferase reporter gene experiment was used to verify miRNA targets. Immunohistochemical assay was used to detect the expression of proteins related to metastasis and apoptosis in tumor tissues. Results. The expression of GAS5 was downregulated in CRC tissues and cell lines. The overexpression of GAS5 can inhibit cell proliferation and progression, induce apoptosis in vitro, and inhibit the growth of CRC tumor in vivo. In contrast, the expression of miR-10b, a downstream target of GAS5, was increased in CRC tissues and cells. Suppression of the miR-10b gene can inhibit proliferation and metastasis and cause apoptosis of CRC cells. In addition, luciferase reports show that GAS5 inhibits the progression of CRC cells by binding to miR-10b. Rescue experiments showed that overexpressed miR-10b could reverse GAS5-mediated antitumor effect on CRC cells in vivo and in vitro. Conclusions. LncRNA GAS5 interacts with miR-10b to inhibit cell proliferation and migration and induces apoptosis in colorectal cancer. GAS5 and miR-10b could become potential therapeutic targets for CRC.